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Sodium iodate-induced retina degeneration observed in non-separate sclerochoroid/retina pigment epithelium/retina whole mounts

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Annals of Eye Science 2022年第1期7卷 16-32页

作者： Soo-Young Kim Yang Zhao Hong-Lim Kim Youngman Oh Qingguo Xu Department of Pharmaceutics Virginia Commonwealth UniversityRichmondVAUSA Department of Biology Virginia Commonwealth UniversityRichmondVAUSA Department of Glaucoma Aier School of OphthalmologyCentral South UniversityChangshaChina Changsha Aier Eye Hospital Aier Eye Hospital GroupChangshaChina Department of Anatomy College of Veterinary MedicineKonkuk UniversitySeoulRepublic of Korea Integrative Research Support Center Laboratory of Electron MicroscopeThe Catholic University of KoreaSeoulRepublic of Korea Department of Pathology School of MedicineVirginia Commonwealth UniversityRichmondVAUSA Massey Cancer Center Virginia Commonwealth UniversityRichmondVAUSA Department of Ophthalmology and Center for Pharmaceutical Engineering and Sciences Virginia Commonwealth UniversityRichmondVAUSA

Background:Sodium iodate(SI)is a chemical widely applied to induce retina degeneration in animal models.SI treatment caused formation of rosettes/folds in the outer nuclear layer(ONL)of the rat retina,but it was previously unclear whether SI also forms rosettes in mice.In addition,SI induced retina degeneration was never addressed in non-separate sclerochoroid/retina pigment epithelium/retina whole mount.Here we displayed features of retina degeneration including rosette formation in mice and developed a morphological analytic assessment using sclerochoroid/retina pigment epithelium/retina whole mounts.Methods:SI was intraperitoneally injected in Sprague-Dawley(SD)rats and C57BL/6J mice using a single dose(50 mg/kg)or with a dose range(10 to 50 mg/kg)in BALB/C mice.Rat retinas were investigated up to 2-week post-injection by histology and whole mounts,and mouse retinas were investigated up to 3-week post-injection by histology,fluorescent staining of sections and/or sclerochoroid/retina pigment epithelium/retina whole mounts for the morphological evaluations of the SI-induced retina damage.Results:SI-induced retina damage caused photoreceptor(PR)degeneration and rosettes/folds formation,as well as retina pigment epithelium degeneration and inward migration.It displayed mixed nuclei from choroid to PRs,due to layer disorganization,as shown by single horizontal images in the sclerochoroid/retina pigment epithelium/retina whole mounts.Measurement of the PR rosette area induced by SI provided a quantitative,morphological evaluation of retina degeneration.Conclusions:The method of non-separate sclerochoroid/retina pigment epithelium/retina whole staining and mount allows us to observe the integral horizontal view of damage from sclera to PR layers,which cannot be addressed by using sectioned and separate whole mount methods.This method is applicable for morphological evaluation of retina damage,especially in the subretinal layer.

关键词： Subretina retina degeneration rosettes age-related macular degeneration(AMD)

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Mutations in a P-type ATPase gene cause axonal and retina degeneration

Mutations in a P-type ATPase gene cause axonal and retina de...

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第十二次全国医学遗传学学术会议

作者： Xianjun Zhu Sichuan Provincial Key Laboratory for Human Gene Study Sichuan Academy of Medical Sciences and Sichuan Provincial People’s Hospital

Purpose Neuronal loss and axonal degeneration are important pathological features of many neurodegenerative diseases.The molecular mechanisms underlying the majority of axonal degeneration conditions remain unknown.To better understand axonal degeneration,we studied a mouse mutant wabbler-lethal(wl).Methods To better understand axonal degeneration,we studied a mouse mutant wabbler-lethal(wl).Standard pathology analysis was applied to the central and peripheral nervous system of wl mice.Positional cloning technique was used to identify the underlying mutations in wl mice.Atp8a2 expression vector was constructed using standard molecular biology technique.Atp8a2 mutations were introduced by site-directed mutagenesis kit. Results Wabbler-lethal(wl) mutant mice develop progressive ataxia with pronounced neurodegeneration in the central and peripheral nervous system.Here we provide clear evidence that wabbler lethal mutants develop an axonopathy,and that this axonopathy is modulated by Wld and Bax mutations.In addition,we have identified the gene harboring the disease-causing mutations as Atp8a2.We studied three wl alleles and found that all result from mutations in the Atp8a2 gene.Our analysis shows that ATP8A2 possesses phosphatidylserine translocase activity and is involved in localization of phosphatidylserine to the inner leaflet of the plasma membrane. Atp8a2 is widely expressed in the brain,the spinal cord,and retina.We assessed two of the mutant alleles of Atp8a2 and found they are both nonfunctional for the phosphatidylserine translocase activity,wl mutant retina displayed degenerated photoreceptors and impaired ERG response. Conclusions Our data demonstrate for the first time that mutation of a mammalian phosphatidylserine translocase causes axon degeneration and photoreceptor degeneration.

关键词： Axonal degeneration retina degeneration wabbler lethal Atp8a2 phosphatidylserine flippase

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Comparison between sodium iodate and lipid peroxide murine models of age-related macular degeneration for drug evaluation-a narrative review

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Annals of Eye Science 2022年第1期7卷 86-105页

作者： Soo-Young Kim Haohua Qian Department of Pharmaceutics Department of BiologyVirginia Commonwealth UniversityRichmondVAUSA Center for Nanomedicine Wilmer Eye InstituteDepartment of OphthalmologyJohns Hopkins University of MedicineBaltimoreMDUSA Visual Function Core National Eye InstituteNational Institutes of HealthBethesdaMDUSA

Objective:In this review,non-transgenic models of age-related macular degeneration(AMD)are discussed,with focuses on murine retinal degeneration induced by sodium iodate and lipid peroxide(HpODE)as preclinical study platforms.Background:AMD is the most common cause of vision loss in a world with an increasingly aging population.The major phenotypes of early and intermediate AMD are increased drusen and autofluorescence,Müller glia activation,infiltrated subretinal microglia and inward moving retinal pigment epithelium(RPE)cells.Intermediate AMD may progress to advanced AMD,characterized by geography atrophy and/or choroidal neovascularization(CNV).Various transgenic and non-transgenic animal models related to retinal degeneration have been generated to investigate AMD pathogenesis and pathobiology,and have been widely used as potential therapeutic evaluation platforms.Methods:Two retinal degeneration murine models induced by sodium iodate and HpODE are described.Distinct pathological features and procedures of these two models are compared.In addition,practical protocol and material preparation and assessment methods are elaborated.Conclusions:retina degeneration induced by sodium iodate and HpODE in mouse eye resembles many clinical aspects of human AMD and complimentary to the existent other animal models.However,standardization of procedure and assessment protocols is needed for preclinical studies.Further studies of HpODE on different routes,doses and species will be valuable for the future extensive use.Despite many merits of murine studies,differences between murine and human should be always considered.

关键词： retina degeneration retinal pigment epithelium(RPE) photoreceptor microglia

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Cell transplantation to replace retinal ganglion cells faces challenges-the Switchboard Dilemma

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Neural Regeneration Research 2021年第6期16卷 1138-1143页

作者： Yuan Liu Richard K.Lee Bascom Palmer Eye Institute University of Miami Miller School of MedicineMiamiFLUSA

The mammalian retina displays incomplete intrinsic regenerative capacities;therefore,retina degeneration is a major cause of irreversible blindness such as glaucoma,agerelated macular degeneration and diabetic retinopathy.These diseases lead to the loss of retinal cells and serious vision loss in the late stage.Stem cell transplantation is a great promising novel treatment for these incurable retinal degenerative diseases and represents an exciting area of regenerative neurotherapy.Several suitable stem cell sources for transplantation including human embryonic stem cells,induced pluripotent stem cells and adult stem cells have been identified as promising target populations.However,the retina is an elegant neuronal complex composed of various types of cells with different functions.The replacement of these different types of cells by transplantation should be addressed separately.So far,retinal pigment epithelium transplantation has achieved the most advanced stage of clinical trials,while transplantation of retinal neurons such as retinal ganglion cells and photoreceptors has been mostly studied in pre-clinical animal models.In this review,we opine on the key problems that need to be addressed before stem cells transplantation,especially for replacing injured retinal ganglion cells,may be used practically for treatment.A key problem we have called the Switchboard Dilemma is a major block to have functional retinal ganglion cell replacement.We use the public switchboard telephone network as an example to illustrate different difficulties for replacing damaged components in the retina that allow for visual signaling.retinal ganglion cell transplantation is confronted by significant hurdles,because retinal ganglion cells receive signals from different interneurons,integrate and send signals to the correct targets of the visual system,which functions similar to the switchboard in a telephone network-therefore the Switchboard Dilemma.

关键词： cell transplantation optic nerve regeneration photoreceptors retina degeneration retinal ganglion cells stem cells

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